Oxygen free radicals in acute pancreatitis of the rat.

Schoenberg, M. H.; Büchler, Markus W.; Gaspar, Miklos; Stinner, A.; Younès, M.; Melzner, Ingo; Bültmann, B.; Beger, H. G.

doi:10.1136/gut.31.10.1138

Cited by 183 publications

(110 citation statements)

References 17 publications

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“…The histological abnormalities in the combined treatment group were significantly less compared with the use of allopurinol and HBO alone, indicating a potentiation of effect. Allopurinol also decreased the oxidative stress parameters, as it has been reported previously [13,14,27,28] , although allopurinol was found to have no effect on the incidence and severity of endoscopic retrograde cholangiopancreatography (ERCP)-induced pancreatitis in studies on human subjects by Budzynska et al [29] . When allopurinol was co-administered with HBO at the same doses, the overall antioxidant effect did not increase.…”

Section: Discussionsupporting

confidence: 63%

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Combination of allopurinol and hyperbaric oxygen therapy: A new treatment in experimental acute necrotizing pancreatitis?

Cömert¹

2007

WJG

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AIM:To investigate the individual and combined effects of allopurinol and hyperbaric oxygen (HBO) therapy on biochemical and histopathological changes, oxidative stress, and bacterial translocation (BT) in the experimental rat acute pancreatitis (AP). METHODS:Eighty-five Sprague-Dawley rats were included in the study. Fifteen of the eighty-five rats were used as controls (sham, GroupⅠ). AP was induced via intraductal taurocholate infusion in the remaining seventy rats. Rats that survived to induction of acute necrotizing pancreatitis were randomized into four groups. Group Ⅱ received saline, Group Ⅲ allopurinol, Group Ⅳ allopurinol plus HBO and Group Ⅴ HBO alone. Serum amylase levels, oxidative stress parameters, BT and histopathologic scores were determined. RESULTS:Serum amylase levels were lower in Groups Ⅲ, Ⅳ and Ⅴ compared to Group Ⅱ (974 ± 110, 384 ± 40, 851 ± 56, and 1664 ± 234 U/L, respectively, P < 0.05, for all). Combining the two treatment options revealed significantly lower median [25-75 percentiles] histopathological scores when compared to individual administrations (13 [12.5-15] in allopurinol group, 9.5 [7-11.75] in HBO group,[6][7].5] in combined group, P < 0.01). Oxidative stress markers were significantly better in all treatment groups compared to the controls. Bacterial translocation into the pancreas and mesenteric lymph nodes was lower in Groups Ⅲ, Ⅳ and Ⅴ compared to Group Ⅱ (54%, 23%, 50% vs 100% for translocation to pancreas, and 62%, 46%, 58% vs 100% for translocation to mesenteric lymph nodes, respectively, P < 0.05 for all). CONCLUSION:The present study confirms the benefit of HBO and allopurinol treatment when administered separately in experimental rat AP. Combination of these treatment options appears to prevent progression of pancreatic injury parameters more effectively.

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Section: Discussionsupporting

confidence: 63%

“…Allopurinol (ALPL) has antioxidant properties, and previous studies have shown that antioxidant therapy reduces tissue injury and bacterial translocation in experimental pancreatitis [13,14] .…”

Section: Introductionmentioning

confidence: 99%

Combination of allopurinol and hyperbaric oxygen therapy: A new treatment in experimental acute necrotizing pancreatitis?

Cömert¹

2007

WJG

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“…Five-micrometer pancreatic sections were dewaxed by xylene, hydrated through a degraded ethanol series, and stained with hematoxylin and eosin. Specimens were evaluated with light microscopy by an expert pathologist who was unaware of groups and rated samples between 0 and 4 for the presence of edema, acinar necrosis, hemorrhage, inflammation, and perivascular infiltration as described by Schoenberg et al (10).…”

Section: Histologic Evaluationmentioning

confidence: 99%

Efficacy of tocilizumab treatment in cerulein-induced experimental acute pancreatitis model in rats

Hancerlı¹,

Kaplan²,

Tanoğlu³

et al. 2017

Turk J Gastroenterol

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“…Acute pancreatitis is a multifactorial disease associated with the release of digestive enzymes to the pancreatic interstitium and the systemic circulation, as well as with increased cytokine production and release (Schoenberg et al, 1990). Cerulein pancreatitis is one of the best-characterized animal models of experimental pancreatitis and exhibits biochemical, morphological, and pathophysiological similarities to various aspects of human pancreatitis (Willemer et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

“…Doses of CCK or cerulein, a cholecystokinin (CCK) analog, beyond those that cause the maximum pancreatic secretion of amylase and lipase Sato et al, 1989) result in pancreatitis. The disease is characterized by dysregulation of the production and secretion of digestive enzymes, particularly the inhibition of pancreatic secretion and an elevation in serum levels, as well as cytoplasmic vacuolization, the death of acinar cells, edema formation, and infiltration of inflammatory cells into the pancreas (Schoenberg et al, 1990;Lerch and Adler, 1995). The key events appear to be a premature, intra-pancreatic activation of digestive enzyme granules, but the earliest events that trigger acute pancreatitis are unclear.…”

Section: Introductionmentioning

confidence: 99%

Altered Gene Expression in Cerulein-Stimulated Pancreatic Acinar Cells: Pathologic Mechanism of Acute Pancreatitis

Lim

Kim

2009

Korean J Physiol Pharmacol

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Acute pancreatitis is a multifactorial disease associated with the premature activation of digestive enzymes. The genes expressed in pancreatic acinar cells determine the severity of the disease. The present study determined the differentially expressed genes in pancreatic acinar cells treated with cerulein as an in vitro model of acute pancreatitis. Pancreatic acinar AR42J cells were stimulated with 10 − 8 M cerulein for 4 h, and genes with altered expression were identified using a cDNA microarray for 4,000 rat genes and validated by real-time PCR. These genes showed a 2.5-fold or higher increase with cerulein: lithostatin, guanylate cyclase, myosin light chain kinase 2, cathepsin C, progestin-induced protein, and pancreatic trypsin 2. Stathin 1 and ribosomal protein S13 showed a 2.5-fold or higher decreases in expression. Real-time PCR analysis showed time-dependent alterations of these genes. Using commercially available antibodies specific for guanylate cyclase, myosin light chain kinase 2, and cathepsin C, a time-dependent increase in these proteins were observed by W estern blotting. Thus, disturbances in proliferation, differentiation, cytoskeleton arrangement, enzyme activity, and secretion may be underlying mechanisms of acute pancreatitis.

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Oxygen free radicals in acute pancreatitis of the rat.

Cited by 183 publications

References 17 publications

Combination of allopurinol and hyperbaric oxygen therapy: A new treatment in experimental acute necrotizing pancreatitis?

Combination of allopurinol and hyperbaric oxygen therapy: A new treatment in experimental acute necrotizing pancreatitis?

Efficacy of tocilizumab treatment in cerulein-induced experimental acute pancreatitis model in rats

Altered Gene Expression in Cerulein-Stimulated Pancreatic Acinar Cells: Pathologic Mechanism of Acute Pancreatitis

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